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Archive - 01 - 2011

Childhood Obesity Linked with Health Habits, Not Heredity

Posted by dlife on Mon, Jan 31, 11, 09:17 AM 0 Comment

January 31, 2011 (Newswise) Are some children genetically tuned to be overweight, or is lifestyle to blame for childhood obesity?Check-ups of 1,003 Michigan 6th graders in a school-based health program showed children who are obese were more likely to consume school lunch instead of a packed lunch from home and spend two hours a day watching TV or playing a video game.The results were compiled by the University of Michigan Cardiovascular Center and suggests unhealthy habits are feeding the childhood obesity trend.For the extremely overweight child, genetic screening may be a consideration, says study senior author Kim A. Eagle, M.D., a cardiologist and a director of the U-M Cardiovascular Center. For the rest, increasing physical activity, reducing recreational screen time and improving the nutritional value of school lunches offers great promise to begin a reversal of current childhood obesity trends.President Obama recently signed the Healthy, Hunger-Free Kids Act of 2010 to create healthier school menus for the 31 million children in the United States who eat lunch through school programs.The act is designed to improve nutrition by reducing salt, fat and sugar in school meals and reduce childhood obesity which has tripled in the U.S. in the past 30 years.The prevalence of obesity among U.S. children ages 6 to 11 has increased from 6.5 percent in 1980 to 19.6 percent in 2008.Children involved in the study participate in Project Healthy Schools, school-based program supported by communities and the U-M Health System to teach middle school students about healthy lifestyles, in hopes of reducing their future risk of cardiovascular disease and diabetes.Project Healthy Schools is available at 13 Michigan middle schools and is one of the few school-based programs to show sustained benefits in reducing cholesterol and high blood pressure among participants.The U-M study was published in the American Heart Journal.U-M researchers found that 58 percent of obese children had watched two hours of TV in the previous day, compared to 41 percent of non-obese children. Forty-five percent of obese students always ate school lunch, but only 34 percent of non-obese students ate school lunch.Significantly fewer obese kids exercised regularly, took physical education classes, or were a member of a sports team.Because the eating and exercise patterns of obese children were so different than their normal weight peers, researchers concluded that lifestyle was more closely linked with childhood obesity, than genetics.New evidence has emerged showing a leptin deficiency, a genetic mutation in the hormone that controls hunger, may cause a person to overeat.If diets and physical activity were similar in obese and non-obese students this would argue for a stronger genetic basis for obesity in children, says study first author Taylor Eagle.In the U-M study, 15 percent of the middle school students were obese, but nearly all, whether overweight or not, reported unhealthy habits.More than 30 percent had consumed regular soda the previous day, and less than half remembered eating two portions of fruits and vegetables within the past 24 hours. Only one-third of students said they exercised for 30 minutes for five days in the previous week.Its clear that opportunities to improve health abound for the majority of our students, not just the 15 percent who are already obese, says study co-author Elizabeth Jackson, M.D., assistant professor of internal medicine at the U-M Cardiovascular Center.

Researchers Discover Root Cause of Blood Vessel Damage in Diabetes

Posted by dlife on Fri, Jan 28, 11, 04:31 PM 0 Comment

January 28, 2011 (Newswise) A key mechanism that appears to contribute to blood vessel damage in people with diabetes has been identified by researchers at Washington University School of Medicine in St. Louis.Blood vessel problems are a common diabetes complication. Many of the nearly 26 million Americans with the disease face the prospect of amputations, heart attack, stroke and vision loss because of damaged vessels.Reporting in the , the Washington University researchers say studies in mice show that the damage appears to involve two enzymes, fatty acid synthase (FAS) and nitric oxide synthase (NOS), that interact in the cells that line blood vessel walls.We already knew that in diabetes theres a defect in the endothelial cells that line the blood vessels, says first author Xiaochao Wei, PhD. People with diabetes also have depressed levels of fatty acid synthase. But this is the first time weve been able to link those observations together.Wei is a postdoctoral research scholar in the lab of Clay F. Semenkovich, MD, the Herbert S. Gasser Professor of Medicine, professor of cell biology and physiology and chief of the Division of Endocrinology, Metabolism and Lipid Research.Wei studied mice that had been genetically engineered to make FAS in all of their tissues except the endothelial cells that line blood vessels. These so-called FASTie mice experienced problems in the vessels that were similar to those seen in animals with diabetes.It turns out that there are strong parallels between the complete absence of FAS and the deficiencies in FAS induced by lack of insulin and by insulin resistance, Semenkovich says.Comparing FASTie mice to normal animals, as well as to mice with diabetes, Wei and Semenkovich determined that mice without FAS, and with low levels of FAS, could not make the substance that anchors nitric oxide synthase to the endothelial cells in blood vessels.Weve known for many years that to have an effect, NOS has to be anchored to the wall of the vessel, Semenkovich says. Xiaochao discovered that fatty acid synthase preferentially makes a lipid that attaches to NOS, allowing it to hook to the cell membrane and to produce normal, healthy blood vessels.In the FASTie mice, blood vessels were leaky, and in cases when the vessel was injured, the mice were unable to generate new blood vessel growth.The actual mechanism involved in binding NOS to the endothelial cells is called palmitoylation. Without FAS, the genetically engineered mice lose NOS palmitoylation and are unable to modify NOS so that it will interact with the endothelial cell membrane. That results in blood vessel problems.In animals that dont have fatty acid synthase and normal nitric oxide synthase in endothelial cells, we saw a lot of leaky blood vessels, Semenkovich explains. The mice also were more susceptible to the consequences of infection, and they couldnt repair damage that occurred problems that also tend to be common in people with diabetes.In one set of experiments, the researchers interrupted blood flow in the leg of a normal mouse and in a FASTie mouse.The control animals regained blood vessel formation promptly, Semenkovich says, but that did not happen in the animals that were modified to be missing fatty acid synthase.Its a long way, however, from a mouse to a person, so the researchers next looked at human endothelial cells, and they found that a similar mechanism was at work.Our findings strongly suggest that if we can use a drug or another enzyme to promote fatty acid synthase activity, specifically in blood vessels, it might be helpful to patients with diabetes, Wei says. We also have been able to demonstrate that palmitoylation of nitric oxide synthase is impaired in diabetes, and if we can find a way to promote the palmitoylation of NOS, even independent of fatty acid synthase, it may be possible to treat some of the vascular complications of diabetes.And it shouldnt matter whether a person has type 1 diabetes and cant manufacture insulin or the more common type 2 diabetes, in which a person becomes resistant to insulin.Thats one of the key findings, Semenkovich says. It wont matter whether its an absence of insulin or resistance to insulin: both are associated with defects in FAS.

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